L Burt Nabors

University of Alabama at Birmingham, Birmingham, Alabama, United States

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Publications (47)284.09 Total impact

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    ABSTRACT: Bevacizumab is widely used for treatment of high-grade gliomas and other malignancies. Because bevacizumab has been shown to be associated with neurocognitive decline, this study is designed to investigate whether prolonged treatment with bevacizumab is also associated with brain atrophy. We identified 12 high-grade glioma patients who received bevacizumab for 12 months at the first recurrence and 13 matched controls and blindly compared the volumes of the contralateral hemispheres and contralateral ventricle in these two groups at baseline and after 12 ± 2 months of the baseline scan by two independent analyses. The volumes of the contralateral hemispheres and ventricles did not differ significantly between the two groups at baseline. Whereas, in the control group the volumes of the contralateral hemisphere changed subtly from baseline to follow-up (p = 0.23), in the bevacizumab-treated group the volumes significantly decreased from baseline to follow-up (p = 0.03). There was significant increase in the contralateral ventricle volume from base line to follow-up scans in both the control group (p = 0.01) and in the bevacizumab group (p = 0.005). Both the absolute and the percentage changes of contralateral hemisphere volumes and contralateral ventricular volumes between the two patient groups were statistically significant (p < 0.05). Results of this study demonstrate prolonged treatment with bevacizumab is associated with atrophy of the contralateral brain hemisphere.
    Journal of Neuro-Oncology 02/2015; DOI:10.1007/s11060-015-1751-z · 3.12 Impact Factor
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    ABSTRACT: The aim of this study was to investigate medical decision-making capacity (MDC) in patients with brain metastases. Participants were 41 adults with brain metastases with Karnofsky Performance Status scores of ≥70 who were recruited from an academic medical center and 41 demographically matched controls recruited from the community. We evaluated MDC using the Capacity to Consent to Treatment Instrument and its four clinically relevant consent standards (expressing a treatment choice, appreciation, reasoning, and understanding). Capacity impairment ratings (no impairment, mild/moderate impairment, and severe impairment) on the consent standards were also assigned to each participant with brain metastasis using cutoff scores derived statistically from the performance of the control group. The brain metastasis patient group performed significantly below controls on consent standards of understanding and reasoning. Capacity compromise was defined as performance ≤1.5 standard deviations below the control group mean. Using this definition, approximately 60% of the participants with brain metastases demonstrated capacity compromise on at least one MDC standard. When defining capacity compromise as performance ≤1.5 standard deviation below the control group mean, over half of patients with brain metastases have reduced capacity to make treatment decisions. This impairment is demonstrated shortly after initial diagnosis of brain metastases and highlights the importance of routine clinical assessment of MDC following diagnosis of brain metastasis. These results also indicate a need for the development and investigation of interventions to support or improve MDC in this patient population. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.
    Psycho-Oncology 01/2015; DOI:10.1002/pon.3753 · 4.04 Impact Factor
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    ABSTRACT: Background We aimed to investigate the relationship between medical decisional capacity (MDC) and Karnofsky Performance Status (KPS) in adults with malignant brain tumors. Methods Participants were 71 adults with primary (n = 26) or metastatic (n = 45) brain tumors. Testing to determine KPS scores and MDC was performed as close together as possible for each patient. Participants were administered a standardized measure of medical decision-making capacity (Capacity to Consent to Treatment Instrument [CCTI]) to assess 3 treatment consent abilities (ie, appreciation, reasoning, and understanding). Capacity classifications (ie, capable, marginally capable, and incapable) were established using cut scores previously derived from healthy control CCTI performance. Results The majority of participants had KPS scores of 90–100 (n = 39), with the remainder divided between KPS scores of 70–80 (n = 26) and 50–60 (n = 6). Comparisons between persons with KPS scores of 90–100 or 70–80 revealed significant differences on the CCTI consent standards of understanding and appreciation. Participants with KPS ratings of 90–100 achieved 46% capable classifications across all CCTI standards, in contrast with 23% of participants with KPS ratings of 70–80, and 0% of participants with KPS ratings of 50–60. Conclusions A substantial portion of brain-tumor patients with KPS scores reflecting only minimal disability nonetheless demonstrated impairments on standardized measures of MDC. Clinicians working with this adult population should carefully screen for capacity to make clinical treatment decisions regardless of functional/performance status.
    12/2014; DOI:10.1093/nop/npu030
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    ABSTRACT: The NCCN Clinical Practice Guidelines in Oncology for Central Nervous System Cancers use radiologic presentation in the initial evaluation of patients with primary brain tumors and in the determination of response to therapy. The dominant modality use is MRI because of its superior image resolution, speed of acquisition, and high safety profile for patients. The interpretation of MRI is a critical aspect of patient care and evaluation. This article reviews the predominant aspects of MRI for brain tumors, the standard sequences, the criteria to consider in determining treatment response, and advanced aspects currently available. The proper integration of this essential imaging modality into patient care ensures timely disease evaluation and guides the use of therapeutic tools.
    Journal of the National Comprehensive Cancer Network: JNCCN 11/2014; 12(11):1561-8. · 4.24 Impact Factor
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    ABSTRACT: Cilengitide is a selective αvβ3 and αvβ5 integrin inhibitor. Data from phase 2 trials suggest that it has antitumour activity as a single agent in recurrent glioblastoma and in combination with standard temozolomide chemoradiotherapy in newly diagnosed glioblastoma (particularly in tumours with methylated MGMT promoter). We aimed to assess cilengitide combined with temozolomide chemoradiotherapy in patients with newly diagnosed glioblastoma with methylated MGMT promoter.
    The Lancet Oncology 08/2014; 15(10). DOI:10.1016/S1470-2045(14)70379-1 · 24.73 Impact Factor
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    ABSTRACT: This phase I/II trial evaluated the maximum tolerated dose (MTD) and pharmacokinetics of afatinib plus temozolomide as well as the efficacy and safety of afatinib as monotherapy (A) or with temozolomide (AT) vs temozolomide monotherapy (T) in patients with recurrent glioblastoma (GBM).
    Neuro-Oncology 08/2014; DOI:10.1093/neuonc/nou160 · 5.29 Impact Factor
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    ABSTRACT: The objective of this study was to evaluate if peritumoral (PT) perfusion parameters obtained from dynamic susceptibility weighted contrast enhanced perfusion MRI can predict overall survival (OS) and progression free survival (PFS) in patients with newly diagnosed glioblastoma multiforme (GBM). Twenty-eight newly diagnosed GBM patients, who were treated with resection followed by concurrent chemoradiation and adjuvant chemotherapy, were included in this study. Evaluated perfusion parameters were pre- and post-treatment PT relative cerebral blood volume (rCBV) and relative cerebral blood flow (rCBF). Proportional hazard analysis was used to assess the relationship OS, PFS and perfusion parameters. Kaplan-Meier survival estimates and log-rank test were used to characterize and compare the patient groups with high and low perfusion parameter values in terms of OS and PFS. Pretreatment PT rCBV and rCBF were not associated with OS and PFS whereas there was statistically significant association of both posttreatment PT rCBV and rCBF with OS and posttreatment rCBV with PFS (association of PFS and posttreatment rCBF was not statistically significant). Neither the Kaplan-Meier survival estimates nor the log-rank test demonstrated any differences in OS between high and low pretreatment PT rCBV values and rCBF values; however, high and low post-treatment PT rCBV and rCBF values did demonstrate statistically significant difference in OS and PFS. Our study found posttreatment, not pretreatment, PT perfusion parameters can be used to predict OS and PFS in patients with newly diagnosed GBM.
    Journal of Neuro-Oncology 08/2014; 120(2). DOI:10.1007/s11060-014-1560-9 · 2.79 Impact Factor
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    ABSTRACT: Cognitive impairment is a common symptom in patients with brain metastasis, and significant cognitive dysfunction is prevalent in a majority of patients who are still able to engage in basic self-care activities. In the current study, the neurocognitive performance of 32 patients with brain metastasis and 32 demographically-matched controls was examined using a battery of standardized neuropsychological tests, with the goal of comprehensively examining the cognitive functioning of newly diagnosed brain metastasis patients. The cognition of all patients was assessed within 1 week of beginning treatment for brain metastasis. Results indicated impairments in verbal memory, attention, executive functioning, and language in relation to healthy controls. Performance in relation to appropriate normative groups was also examined. Overall, cognitive deficits were prevalent and memory was the most common impairment. Given that cognitive dysfunction was present in this cohort of patients with largely minimal functional impairment, these results have implications for patients, caregivers and health care providers treating patients with brain metastasis.
    Journal of Neuro-Oncology 07/2014; 120(1). DOI:10.1007/s11060-014-1543-x · 2.79 Impact Factor
  • Louis Burt Nabors, Natalia Filippova, Xiuhua Yang
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    ABSTRACT: The RNA-binding protein, HuR is over-expressed in glioma and controls mRNA stabilization and translation in centrosomes. Alterations in HuR phosphorylation promote centrosomal abnormalities.
    Neuro-Oncology 07/2014; 16 Suppl 3:iii20. DOI:10.1093/neuonc/nou206.74 · 5.29 Impact Factor
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    ABSTRACT: Src family kinases (SFKs) are highly expressed and active in clinical glioblastoma multiforme (GBM) specimens. SFKs inhibitors have been demonstrated to inhibit prolifer-ation and migration of glioma cells. However, the role of SFKs in glioma stem cells (GSCs), which are important for treatment resistance and recurrence, has not been reported. Here, we examined the expression pattern of individual members of SFKs and their functional role in CD133+ GSCs in comparison to primary glioma cells. We found that Fyn, c-Src and Yes were robustly expressed in GSCs while Lck was absent. Knockdown of c-Src, Yes or treatment with the SFK inhibitor dasatinib inhibited the migration of GSCs, but had no impact on their growth or self-renewal. These results suggest that SFKs represent an effective target for GSC migration but not for their growth.
    International Journal of Oncology 05/2014; 45(1). DOI:10.3892/ijo.2014.2432 · 2.77 Impact Factor
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    ABSTRACT: Protein arginine methyltransferase 5 (PRMT5) catalyzes the formation of ω-NG,N'G-symmetric dimethylarginine residues on histones as well as other proteins. These modifications play an important role in cell differentiation and tumor cell growth. However, the role of PRMT5 in human glioma cells has not been characterized. In this study, we assessed protein expression profiles of PRMT5 in control brain, WHO grade II astrocytomas, anaplastic astrocytomas, and glioblastoma multiforme (GBM) by immunohistochemistry. PRMT5 was low in glial cells in control brain tissues and low grade astrocytomas. Its expression increased in parallel with malignant progression, and was highly expressed in GBM. Knockdown of PRMT5 by small hairpin RNA caused alterations of p-ERK1/2 and significantly repressed the clonogenic potential and viability of glioma cells. These findings indicate that PRMT5 is a marker of malignant progression in glioma tumors and plays a pivotal role in tumor growth.
    Journal of Neuro-Oncology 03/2014; 118(1). DOI:10.1007/s11060-014-1419-0 · 3.12 Impact Factor
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    ABSTRACT: G207, a mutant herpes simplex virus (HSV) type 1, is safe when inoculated into recurrent malignant glioma. We conducted a phase I trial of G207 to demonstrate the safety of stereotactic intratumoral administration when given 24 hours prior to a single 5Gy radiation dose in patients with recurrent malignant glioma. Nine patients with progressive, recurrent malignant glioma despite standard therapy were included. Patients received one dose of G207 stereotactically inoculated into the multiple sites of the enhancing tumor margin, then treated focally with 5 Gy radiation. Treatment was well tolerated and no patient developed HSV encephalitis. The median interval between initial diagnosis and G207 inoculation was 18 months (mean 23, range, 11-51 months). Six of nine patients had stable disease or partial response for a least one timepoint. Three instances of marked radiographic response to treatment occurred. The median survival time from G207 inoculation until death was 7.5 months (95% CI, 3.0- 12.7). In conclusion, this study showed the safety and the potential for clinical response of single dose oncolytic HSV therapy augmented with radiation in the treatment of malignant glioma patients. Additional studies with oncolytic HSV such as G207 in the treatment of human glioma are recommended.Molecular Therapy (2014); doi:10.1038/mt.2014.22.
    Molecular Therapy 02/2014; DOI:10.1038/mt.2014.22 · 6.43 Impact Factor
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    ABSTRACT: PURPOSEA randomized, phase III, placebo-controlled, partially blinded clinical trial (REGAL [Recentin in Glioblastoma Alone and With Lomustine]) was conducted to determine the efficacy of cediranib, an oral pan-vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor, either as monotherapy or in combination with lomustine versus lomustine in patients with recurrent glioblastoma. PATIENTS AND METHODS Patients (N = 325) with recurrent glioblastoma who previously received radiation and temozolomide were randomly assigned 2:2:1 to receive (1) cediranib (30 mg) monotherapy; (2) cediranib (20 mg) plus lomustine (110 mg/m(2)); (3) lomustine (110 mg/m(2)) plus a placebo. The primary end point was progression-free survival based on blinded, independent radiographic assessment of postcontrast T1-weighted and noncontrast T2-weighted magnetic resonance imaging (MRI) brain scans.ResultsThe primary end point of progression-free survival (PFS) was not significantly different for either cediranib alone (hazard ratio [HR] = 1.05; 95% CI, 0.74 to 1.50; two-sided P = .90) or cediranib in combination with lomustine (HR = 0.76; 95% CI, 0.53 to 1.08; two-sided P = .16) versus lomustine based on independent or local review of postcontrast T1-weighted MRI. CONCLUSION This study did not meet its primary end point of PFS prolongation with cediranib either as monotherapy or in combination with lomustine versus lomustine in patients with recurrent glioblastoma, although cediranib showed evidence of clinical activity on some secondary end points including time to deterioration in neurologic status and corticosteroid-sparing effects.
    Journal of Clinical Oncology 08/2013; 31(26). DOI:10.1200/JCO.2012.47.2464 · 17.88 Impact Factor
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    ABSTRACT: Malignant gliomas rely on the production of certain critical growth factors including VEGF, interleukin (IL)-6 and IL-8, to fuel rapid tumor growth, angiogenesis, and treatment resistance. Post-transcriptional regulation through adenine and uridine-rich elements of the 3' untranslated region is one mechanism for upregulating these and other growth factors. In glioma cells, we have shown that the post-transcriptional machinery is optimized for growth factor upregulation secondary to overexpression of the mRNA stabilizer, HuR. The negative regulator, tristetraprolin (TTP), on the other hand, may be suppressed because of extensive phosphorylation. Here we test that possibility by analyzing the phenotypic effects of a mutated form of TTP (mt-TTP) in which 8 phosphoserine residues were converted to alanines. We observed a significantly enhanced negative effect on growth factor expression in glioma cells at the post-transcriptional and transcriptional levels. The protein became stabilized and displayed significantly increased antiproliferative effects compared to wild-type TTP. Macroautophagy was induced with both forms of TTP, but inhibition of autophagy did not affect cell viability. We conclude that glioma cells suppress TTP function through phosphorylation of critical serine residues which in turn contributes to growth factor upregulation and tumor progression.
    Journal of Neuro-Oncology 03/2013; DOI:10.1007/s11060-013-1112-8 · 3.12 Impact Factor
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    ABSTRACT: PURPOSE: Increased mitogenic signaling and angiogenesis, frequently facilitated by somatic activation of EGFR (ErbB1) and/or loss of PTEN, and VEGF overexpression, respectively, drive malignant glioma growth. We hypothesized that recurrent glioblastoma patients would exhibit differential antitumor benefit based on tumor PTEN/EGFRvIII status when treated with the antiangiogenic agent pazopanib and the ErbB inhibitor lapatinib. Methods: A Phase II study evaluated the antitumor activity of pazopanib 400 mg/day plus lapatinib 1000 mg/day in patients with grade IV malignant glioma and known PTEN/EGFRvIII status not receiving enzyme-inducing anticonvulsants (EIACs). The Phase II study used a 2-stage Green-Dahlberg design for futility. An independent, parallel Phase I component determined the maximum tolerated regimen (MTR) of pazopanib and lapatinib in grade III/IV glioma patients receiving EIACs. RESULTS: The 6-month progression-free survival rates in Phase II (n=41) were 0% and 15% in the PTEN/EGFRvIII-positive and PTEN/EGFRvIII-negative cohorts, respectively, leading to early termination. Two patients (5%) had a partial response and 14 patients (34%) had stable disease lasting ≥8 weeks. In Phase I (n=34), the MTR was not reached. Based on pharmacokinetic and safety review, a regimen of pazopanib 600 mg plus lapatinib 1000 mg, each twice daily, was considered safe. Concomitant EIACs reduced exposure to pazopanib and lapatinib. CONCLUSIONS: The antitumor activity of this combination at the Phase II dose tested was limited. Pharmacokinetic data indicated that exposure to lapatinib was subtherapeutic in the Phase II evaluation. Evaluation of intratumoral drug delivery and activity may be essential for hypothesis-testing trials with targeted agents in malignant glioma.
    Clinical Cancer Research 01/2013; 19(4). DOI:10.1158/1078-0432.CCR-12-1707 · 8.19 Impact Factor
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    ABSTRACT: Background The signal transduction pathways of epidermal growth factor receptor and Ras are both important in the growth of glioblastoma multiforme (GBM). We hypothesized that inhibition of both pathways would improve the survival time of patients with recurrent GBM.Methods Patients with recurrent/progressive GBM with 0-2 prior chemotherapy regimens received erlotinib 150 mg once daily and sorafenib 400 mg twice daily until progression. The primary endpoint was overall survival. Pharmacokinetic sampling was performed during cycle 1.ResultsThe median overall survival was 5.7 months. Progression-free survival at 6 months was 14%. Toxicity was manageable. Clearance of erlotinib was markedly enhanced by sorafenib.Conclusion The study did not meet its objective of a 30% increase in overall survival time compared with historical controls. Erlotinib and sorafenib have significant pharmacokinetic interactions that may negatively impact the efficacy of the combination regimen.
    Neuro-Oncology 01/2013; DOI:10.1093/neuonc/nos322 · 5.29 Impact Factor
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    ABSTRACT: BACKGROUND: Cilengitide is a selective integrin inhibitor that is well tolerated and has demonstrated biologic activity in patients with recurrent malignant glioma. The primary objectives of this randomized phase 2 trial were to determine the safety and efficacy of cilengitide when combined with radiation and temozolomide for patients with newly diagnosed glioblastoma multiforme and to select a dose for comparative clinical testing. METHODS: In total, 112 patients were accrued. Eighteen patients received standard radiation and temozolomide with cilengitide in a safety run-in phase followed by a randomized phase 2 trial with 94 patients assigned to either a 500 mg dose group or 2000 mg dose group. The trial was designed to estimate overall survival benefit compared with a New Approaches to Brain Tumor Therapy (NABTT) Consortium internal historic control and data from the published European Organization for Research and Treatment of Cancer (EORTC) trial EORTC 26981. RESULTS: Cilengitide at all doses studied was well tolerated with radiation and temozolomide. The median survival was 19.7 months for all patients, 17.4 months for the patients in the 500 mg dose group, 20.8 months for patients in the 2000 mg dose group, 30 months for patients who had methylated O6-methylguanine-DNA methyltransferase (MGMT) status, and 17.4 months for patients who had unmethylated MGMT status. For patients aged ≤70 years, the median survival and survival at 24 months was superior to what was observed in the EORTC trial (20.7 months vs 14.6 months and 41% vs 27%, respectively; P = .008). CONCLUSIONS: Cilengitide was well tolerated when combined with standard chemoradiation and may improve survival for patients newly diagnosed with glioblastoma multiforme regardless of MGMT methylation status. The authors concluded that, from an efficacy and safety standpoint, future trials of this agent in this population should use the 2000 mg dose. Cancer 2012. © 2012 American Cancer Society.
    Cancer 11/2012; 118(22). DOI:10.1002/cncr.27585 · 5.20 Impact Factor
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    ABSTRACT: Primary angiosarcoma of the brain is extremely rare; only 15 cases have been reported in adults over the last 25 years. We describe two cases of primary angiosarcoma of the brain that are well characterized by imaging, histopathology, and immunohistochemistry. Case 1: our first patient was a 35-year-old woman who developed exophthalmos. Subtotal resection of a left extra-axial retro-orbital mass was performed. Case 2: our second patient was a 47-year-old man who presented to our facility with acute visual loss, word-finding difficulty and subtle memory loss. A heterogeneously-enhancing left sphenoid wing mass was removed. We also review the literature aiming at developing a rational approach to diagnosis and treatment, given the rarity of this entity. Gross total resection is the standard of care for primary angiosarcoma of the brain. Adjuvant radiation and chemotherapy are playing increasingly recognized roles in the therapy of these rare tumors.
    Journal of Medical Case Reports 08/2012; 6(1):251. DOI:10.1186/1752-1947-6-251
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: Hu antigen R (HuR) is an mRNA-binding protein belonging to the ELAV family. It is highly expressed in cancer and involved in cell survival and proliferation. The impact of post-translational regulation of HuR and resulting cellular effects are poorly understood. In the current report, we describe a direct interaction between HuR and Cdk5 in glioma. We determined that Cdk5 specifically phosphorylates HuR at the serine 202 residue in the unique hinge region. The molecular consequences of this interaction are an altered HuR ability to bind, stabilize, and promote translation of mRNAs. At the cellular level, the anomalous HuR phosphorylation at this site evokes robust defects in centrosome duplication and cohesion as well as arrest of cell cycle progression. Subcellular fractionation and immunofluorescence technique confirm a direct integration of HuR and Cdk5 with centrosomes. We propose that HuR stores mRNA in the centrosome and that HuR phosphorylation by Cdk5 controls de novo protein synthesis in near proximity to centrosomes and, thus, impacts centrosome function.
    Journal of Biological Chemistry 07/2012; 287(38):32277-87. DOI:10.1074/jbc.M112.353912 · 4.60 Impact Factor
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    ABSTRACT: Glioblastoma is a devastating, incurable disease with few known prognostic factors. Here, we present the first genome-wide survival and validation study for glioblastoma. Cox regressions for survival with 314,635 inherited autosomal single-nucleotide polymorphisms (SNP) among 315 San Francisco Adult Glioma Study patients for discovery and three independent validation data sets [87 Mayo Clinic, 232 glioma patients recruited from several medical centers in Southeastern United States (GliomaSE), and 115 The Cancer Genome Atlas patients] were used to identify SNPs associated with overall survival for Caucasian glioblastoma patients treated with the current standard of care, resection, radiation, and temozolomide (total n = 749). Tumor expression of the gene that contained the identified prognostic SNP was examined in three separate data sets (total n = 619). Genotype imputation was used to estimate hazard ratios (HR) for SNPs that had not been directly genotyped. From the discovery and validation analyses, we identified a variant in single-stranded DNA-binding protein 2 (SSBP2) on 5q14.1 associated with overall survival in combined analyses (HR, 1.64; P = 1.3 × 10(-6)). Expression of SSBP2 in tumors from three independent data sets also was significantly related to patient survival (P = 5.3 × 10(-4)). Using genotype imputation, the SSBP2 SNP rs17296479 had the strongest statistically significant genome-wide association with poorer overall patient survival (HR, 1.79; 95% CI, 1.45-2.22; P = 1.0 × 10(-7)). The minor allele of SSBP2 SNP rs17296479 and the increased tumor expression of SSBP2 were statistically significantly associated with poorer overall survival among glioblastoma patients. With further confirmation, previously unrecognized inherited variations influencing survival may warrant inclusion in clinical trials to improve randomization. Unaccounted for genetic influence on survival could produce unwanted bias in such studies.
    Clinical Cancer Research 04/2012; 18(11):3154-62. DOI:10.1158/1078-0432.CCR-11-2778 · 8.19 Impact Factor

Publication Stats

2k Citations
284.09 Total Impact Points


  • 2004–2014
    • University of Alabama at Birmingham
      • • Department of Neurobiology
      • • Department of Neurology
      • • Department of Biomedical Engineering
      Birmingham, Alabama, United States
  • 2008
    • Duke University Medical Center
      • Division of Neurosurgery
      Durham, North Carolina, United States
    • Baylor University
      Waco, Texas, United States
  • 2006
    • Mayo Clinic - Rochester
      • Department of Neurology
      Rochester, Minnesota, United States
  • 2005
    • Minneapolis Veterans Affairs Hospital
      Minneapolis, Minnesota, United States